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Consequences of transient hippocampal blood brain barrier damage after stroke| old_uid | 10229 |
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| title | Consequences of transient hippocampal blood brain barrier damage after stroke |
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| start_date | 2015/12/04 |
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| schedule | 12h30 |
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| online | no |
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| location_info | salle 01-02 |
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| details | séminaire d’équipe. Invité par Richard Miles |
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| summary | We have shown that opening of the blood brain barrier leads to uptake of albumin by astrocytes and multiple changes in gene expression (with A Friedman). Both K buffering and glutamate homeostasis are disturbed. TGFß receptor blockade suppresses many of the changes in gene regulation. We now ask whether similar changes occur in a model of cortical stroke: Is there a penumbra surround after photothrombotic stroke? Does stroke alter K homeostasis and trigger seizures? Is synaptic plasticity in the hippocampus modified?
Transient blood brain barrier opening in this stroke model induced vasogenic edema in hippocampus and cytotoxic edema in cortex. Post stroke seizures were detected in most (70 %) animals and slices from stroke animals, exposed to serum like electrolytes, generated seizure like events which evolved into spreading depression. They were associated with abnormal potassium accumulation and also detected in animals exposed to intraventricular albumin. Neuronal input-output curves and paired pulse stimulation were altered. LTP induction at low stimulus frequencies was facilitated, while depotentiation was depressed and LTD could not be induced. Some, but not all, of these changes were suppressed by antibodies against TGFßRII receptors. Thus transient blood brain barrier opening induces persistent changes in synaptic plasticity which may facilitate epileptic activities. |
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| responsibles | Oliviero |
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